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More than a hundred years of extensive studies have led to the development of clinically valid animal models of spinal cord injury (SCI) used to investigate neurophysiological mechanisms, pathology and potential therapies. The cat and rat models of SCI were found particularly useful due to several behavioral responses that correspond to clinical symptoms seen in patients. This review concentrates on recovery of motor behavior in the rat and cat models of thoracic spinal cord injury. At the beginning an outline of the general concept of neural control of locomotion: the existence of a spinal network producing the locomotor activity and the supraspinal and sensory inputs that influence this network is presented. Next, the severity of functional impairment in relation to the extent and precise location of lesions at the thoracic level in cats and rats is described. Finally, the impact of animal studies on the treatment of SCI patients and the possibility that a spinal network producing the locomotor activity also exists in humans is discussed.
Lateral hemisection of the spinal cord at the low thoracic level in rats causes severe deterioration of hindlimb locomotor movements followed by the substantial improvements of locomotor functions. However the rate and the level of this improvement remain disputable. In this study we investigated the time course of locomotor recovery analyzing spatial indices of locomotion obtained with CatWalk Gait Analysis System. The animals started to be tested in the CatWalk System two weeks after the injury, when hindlimb plantar stepping recovered. Within first 2 weeks hindlimb locomotor function recovered substantially, and the analyzed locomotor indices reached plateau about one month after injury. Nevertheless, most of the indices, like speed of locomotion, hindlimb base of support, hindlimb abduction did not reached the level obtained before the injury. Within next few months some of them remained at the same level, but 5 months after the hemisection locomotion again started to deteriorate, as was manifested by decrease of locomotor velocity and increase of hindlimb base of support. This study shows that after lateral hemisection of the spinal cord at the low thoracic level the recovery of locomotor functions is limited and that 5 months after the injury the secondary deterioration of locomotion is observed.
Lateral thoracic hemisection of the spinal cord in adult rats results in initial severe impairment of hindlimb movements followed by a relatively fast improvement of locomotor functions. There are data showing substantial or even complete recovery of locomotor performance within 21 – 30 days after spinal cord injury. In our previous study we showed that improvement of locomotor performance reached plateau about four weeks after the injury but animals did not show the full locomotor recovery. The aim of present study was to analyze the time course of relationships between activity of flexors and extensors of each of four limbs during locomotion after lateral hemisection of the spinal cord in rats. The locomotion was tested in freely moving animals walking at speed 0.4 – 1.0 m/s. Bipolar EMG electrodes for the chronic recordings were implanted in soleus and tibialis muscles of hindlimbs and biceps and triceps of forelimbs. The EMG recordings were performed once a week up to six weeks after spinal cord injury. Our results showed that 7 days after the lateral hemisection of the spinal cord the relationship between flexor and extensor muscle (intralimb coordination) of hindlimbs was severely impaired. Moreover, analysis of interlimb coordination revealed that relationships between forelimbs and hindlimbs and hindlimbs themselves were also impaired. Two weeks after surgery the relationships between flexor and extensor muscle of right as well as left hindlimb returned to normal. Diagonal coordination between left forelimb and right hindlimb was also similar to that before the lesion. Only coordination between left hindlimb and remaining three limbs was impaired through the whole period of the study (six weeks after surgery). This results confirmed hypothesis, that after lateral thoracic hemisection of the spinal cord rats did not show the full locomotor recovery.
Marceli Nencki was a great Polish scientist of the XIX century. He began his research at the University of Berne, Switzerland, in 1872. In 1876 he was appointed Associate Professor there, and one year later he became a full Professor and Director of the Institute of Medical Chemistry. In 1891 Marceli Nencki accepted an invitation to organize, together with Ivan P. Pavlov, the Institute of Experimental Medicine in St. Petersburg, where he spent the last decade of his life. In research he concentrated on topics related to urea synthesis, the chemistry of purines, and biological oxidation of aromatic compounds. He also examined the structure of proteins, enzymatic processes in the intestine, and bacterial biochemistry. Among Nencki’s greatest successes was showing, together with Leon Marchlewski, a close chemical relationship between hemoglobin and chlorophyll. The idea to establish the research institute named after Marceli Nencki was born shortly after his death in 1901. Among his friends who pushed forward this idea, the most effective was Nadine Sieber-Shumova, his close co-worker from Berne and St. Petersburg. However, many years were to pass until fi nally in 1918/19 the Nencki Institute was founded. Today, the Nencki Institute, where the neurobiology, neurophysiology, biochemistry and cell biology are widely represented, is the only research centre in Poland where the investigations are performed from the molecular to the whole animal and human subject level.
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